"Good" cholesterol drug doesn’t reduce risks in heart patients
American Heart Association Late-Breaking Clinical Trial Report - Embargoed until 11:30 a.m. PT / 2:30 p.m. ET
November 05, 2012
Study Highlights:
- A drug that raises high-density lipoprotein (HDL – “good”) cholesterol levels didn’t help reduce the risk for another heart event or stroke in patients who had recently experienced an acute coronary syndrome.
- Researchers question whether HDL cholesterol is still an important factor in patients who are already taking medicines to reduce “bad” cholesterol and other cardiovascular risk factors.
LOS ANGELES, Nov. 5, 2012 — Among patients who had a recent heart attack 
or hospitalization for chest pain , a drug that boosts high-density lipoprotein (HDL) cholesterol levels, the so-called “good” cholesterol, failed to reduce the risk of further cardiovascular events, according to a late-breaking clinical trial presented at the American Heart Association’s Scientific Sessions 2012.
or hospitalization for chest pain , a drug that boosts high-density lipoprotein (HDL) cholesterol levels, the so-called “good” cholesterol, failed to reduce the risk of further cardiovascular events, according to a late-breaking clinical trial presented at the American Heart Association’s Scientific Sessions 2012.The Effects of the Cholesteryl Ester Transfer Protein Inhibitor Dalcetrapib in Patients with Recent Acute Coronary Syndrome (dal OUTCOMES) is also published in the New England Journal of Medicine.
Dalcetrapib increased levels of HDL cholesterol by about 30 percent. However, among nearly 16,000 patients followed for an average of about 2 ½ years, this HDL cholesterol boost didn’t reduce patients’ risk of death, another heart attack, hospitalization for heart-related chest pain, or stroke.
Researchers ended the study in May, when an interim analysis showed that the drug neither provided the expected benefit, nor caused harm.
Many studies have shown that low levels of HDL in the bloodstream are associated with a higher risk of heart disease and stroke. However, the role, if any, for drugs that raise HDL is less certain. “Sometimes a study advances scientific knowledge even though it does not advance therapeutic options,” said Gregory Schwartz, M.D., Ph.D., lead study author. “I believe this study did just that by providing an unexpected answer to an important scientific question.”
Dalcetrapib is a cholesteryl ester transfer protein (CETP) inhibitor. Drugs in this class block the transfer of cholesterol from HDL to low-density lipoprotein (LDL, or “bad” cholesterol), thereby raising the levels of HDL in the bloodstream.
Researchers will undoubtedly debate why the treatment didn’t work, which may have a bearing on other drugs in the CETP class that remain under investigation, said Schwartz, chief of the Cardiology Section at Denver VA Medical Center and Professor of Medicine at the University of Colorado in Denver.
Most of the patients studied were also being treated with statin drugs to lower LDL cholesterol, as well as other medications to reduce risk after heart attack, such as aspirin, clopidogrel, and beta blockers.
“It’s possible that when patients are treated with all these risk-reducing drugs, HDL cholesterol level is no longer a risk factor,” said Schwartz. “It’s also possible that HDL is protective in healthy persons, but is altered in patients with heart disease so that it no longer serves the same protective function. Or, it may be that the specific way that dalcetrapib raises HDL is not advantageous.”
Researchers randomly assigned 15,871 patients age 45 and older in 27 countries to take either 600 milligrams of dalcetrapib or a placebo daily. Ninety-seven percent also took aspirin and statins, and 87 percent took beta blockers to reduce the risk of heart complications.
Launched in 2008, the study had average follow-up of 31 months. Although patients taking dalcetrapib had higher HDL levels, 8.3 percent had a major cardiovascular event, compared with 8 percent of the placebo group.Factors such as gender, age, smoking status, medical history, geographical location or body mass index didn’t influence the results, researchers said.
More research is needed to better understand how HDL functions in healthy people compared with patients who have cardiovascular disease, and to learn how CETP inhibitors affect the composition and function of HDL.
In the meantime, there has been no medicine to date that has shown improved outcomes by raising HDL in patients such as these.
“Perhaps the focus should be not so much on raising the level of HDL cholesterol, but on modifying or eliminating the risk factors that are associated with low HDL cholesterol, such as smoking, obesity, diabetes, and sedentary lifestyle.”
Study co-authors are Anders G. Olsson, M.D., Ph.D.; Markus Abt, Ph.D.; Christie M. Ballantyne, M.D.; Philip Barter, M.D., Ph.D.; Jochen Brumm, Ph.D.; Bernard R. Chaitman, M.D.; Ingar M. Holme, Ph.D.; David Kallend, M.B.B.S.; Lawrence A. Leiter, M.D.; Eran Leitersdorf, M.D.; John J.V. McMurray, M.D.; Hardi Mundl, M.D.; Stephen J. Nicholls, M.B.B.S., Ph.D.; Prediman K. Shah, M.D.; Jean-Claude Tardif, M.D.; and R. Scott Wright, M.D.
F. Hoffmann-La Roche, Ltd. funded the study.
Disclosures are here http://newsroom.heart.org/pr/aha/document/DISCLOSURES.pdf 
Follow news from the American Heart Association’s Scientific Sessions 2012 via Twitter: @HeartNews.
###
Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at www.heart.org/corporatefunding .
.Note: The Dal OUTCOMES presentation is at 11:30am PT, Monday, Nov. 5, in Hall G.
For Media Inquiries:
AHA News Media in Dallas: (214) 706-1173
AHA News Media Office, Nov. 3-7,
at the Los Angeles Convention Center: (213) 743-6205
For Public Inquiries: (800) AHA-USA1 (242-8721)
No hay comentarios:
Publicar un comentario